Homocysteine and its thiolactone may promote apoptotic events in blood platelets<i>in vitro</i>

Olas, Beata; Malinowska, Joanna; Rywaniak, Joanna

doi:10.3109/09537104.2010.501119

Cited by 10 publications

(3 citation statements)

References 52 publications

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“…Неблагоприятные эффекты гомоцистеина при метаболических нарушениях опосредуются через различные факторы гиперкоагуляции [5,22]. Данные мировой литературы указывают на значительное увеличение уровня фибриногена, числа тромбоцитов и высвобождаемых ими прокоагулянтных микрочастиц в ответ на введение гомоцистеина [23][24][25][26], однако результаты исследований в отношении показателей тромбодинамики при ГГЦ спорны. По данным R. Marchi и соавт., уровень гомоцистеина в крови не оказывает значимого влияния на показатели тромбодинамики [27].…”

Section: Discussionunclassified

Assessment of Hemostasis System and Factors Associated With Hypercoagulation in Men With Metabolic Syndrome and Initial Decrease of Glomerular Filtration Rate

Худякова¹,

Беззубова²,

Пчелин³

et al. 2017

Nefrologiâ (St.-Peterbg.)

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THE AIM. To assess hypercoagulation factors in men with initial decrease of glomerular filtration rate (IDGFR) and metabolic syndrome (MS) depending on carbohydrate metabolism disorders (CMD). PATIENTS AND METHODS. The study included 79 men with IDGFR and MS. Two groups were assessed: main – patients IDGFR and CMD with MS (n=44) and control group – with IDGFR and MS without CMD (n=35). Besides examinations for confirming IDGFR and CMD type specification all patients were performed following tests: estimated thrombodynamics factors, serum concentration of common testosterone (CT), leptin (L), adiponectin (A), D-dimer (DD), activated platelets count (CD41+CD62P+) (APC), PAI-1, homocysteine (H). We also studied polymorphism of the genes associated with hyperhomocysteinemia (HHC). RESULTS. 90% cases of hyperhomocysteinemia (HHC) in men with IDGFR and MS were associated with genetic defects in enzyme systems regulating this amino acid metabolism.. Patients from the main group in comparison with the subjects without CMD had significantly higher density of the fibrin clot (28012,21±1013,60 vs. 25209,15±1176,90 c.u., р<0,05), serum levels of PAI-1 (78,78±13,00 vs. 43,66±4,00 ng/ml, p<0,01), leptin (13,56±1,40 vs. 8,95±1,60 ng/ml, p<0,01) and lower serum concentration of CT (11,54±0,70 vs. 14,50±1,10 nmol/l, p<0,05). In men with IDGFR and MS with CMD we found positive correlations between activated platelets count and fasting glucose (rs=0,4; р<0,05), activated platelets count and postprandial glucose (rs=0,5; р<0,05), PAI-1 and adiponectin (rs=0,4; р<0,05), PAI-1 and leptin (rs=0,4; р<0,05), homocysteine and MCH (rs=0,5; р<0,05), homocysteine and density of the fibrin clot (rs=0,5; р<0,05), insulin and PAI-1 (rs=0,4; р<0,05), adiponectin and density of the fibrin clot (rs=0,4; р<0,05), hemoglobin and clot growth rate (rs=0,4; р<0,05), RDW and D-dimer (rs=0,4; р<0,05), RDW and density of the fibrin clot (rs=0,6; р<0,05); a negative correlation – between fasting glucose and adiponectin (rs= -0,4; р<0,05). CONCLUSION. CMD in men with IDGFR and MS are associated with procoagulant status via direct and indirect influence on hypercoaculation factors. The role of adiponectin in thrombogenesis is controversial and requires further investigations.

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Section: Discussionunclassified

Assessment of Hemostasis System and Factors Associated With Hypercoagulation in Men With Metabolic Syndrome and Initial Decrease of Glomerular Filtration Rate

Худякова¹,

Беззубова²,

Пчелин³

et al. 2017

Nefrologiâ (St.-Peterbg.)

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“…104 Others showed that homocysteine rather leads to apoptosis of human platelets as it dose-dependently increased phosphatidyl serine exposure, microparticle formation, mitochondrial membrane depolarization, and caspase activation. 143,144 Indoles and Derivates Indoxyl sulfate, a tryptophan metabolite, has prothrombotic properties. It enhanced platelet reactivity toward collagen stimuli via p38-MAPK signaling in mouse platelets.…”

Section: Protein-bound Compounds Advanced Glycation End Products and ...mentioning

confidence: 99%

Section: Uremic Toxin-induced Platelet Abnormalitiesmentioning

confidence: 99%

Platelet Function in CKD: A Systematic Review and Meta-Analysis

Baaten

Sternkopf

Henning

et al. 2021

JASN

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BackgroundPatients with CKD are at high risk for thrombotic and hemorrhagic complications. Abnormalities in platelet function are central to these complications, but reports on platelet function in relation to CKD are conflicting, and vary from decreased platelet reactivity to normal or increased platelet responsiveness. The direct effects of uremic toxins on platelet function have been described, with variable findings.MethodsTo help clarify how CKD affects platelet function, we conducted a systematic review and meta-analysis of platelet activity in CKD, with a focus on nondialysis-induced effects. We also performed an extensive literature search for the effects of individual uremic toxins on platelet function.ResultsWe included 73 studies in the systematic review to assess CKD’s overall effect on platelet function in patients; 11 of them described CKD’s effect on ex vivo platelet aggregation and were included in the meta-analysis. Although findings on platelet abnormalities in CKD are inconsistent, bleeding time was mostly prolonged and platelet adhesion mainly reduced. Also, the meta-analysis revealed maximal platelet aggregation was significantly reduced in patients with CKD upon collagen stimulation. We also found that relatively few uremic toxins have been examined for direct effects on platelets ex vivo; ex vivo analyses had varying methods and results, revealing both platelet-stimulatory and inhibitory effects. However, eight of the 12 uremic toxins tested in animal models mostly induced prothrombotic effects.ConclusionsOverall, most studies report impaired function of platelets from patients with CKD. Still, a substantial number of studies find platelet function to be unchanged or even enhanced. Further investigation of platelet reactivity in CKD, especially during different CKD stages, is warranted.

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Antioxidants and Therapeutic Options of Hyperhomocysteinemia

Khan

Ashraf

2021

Nutritional Management and Metabolic Aspects of Hyperhomocysteinemia

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Homocysteine and its thiolactone may promote apoptotic events in blood plateletsin vitro

Cited by 10 publications

References 52 publications

Assessment of Hemostasis System and Factors Associated With Hypercoagulation in Men With Metabolic Syndrome and Initial Decrease of Glomerular Filtration Rate

Assessment of Hemostasis System and Factors Associated With Hypercoagulation in Men With Metabolic Syndrome and Initial Decrease of Glomerular Filtration Rate

Platelet Function in CKD: A Systematic Review and Meta-Analysis

Antioxidants and Therapeutic Options of Hyperhomocysteinemia

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